Luminal peroxides in intestinal thiol-disulfide balance and cell turnover.
Dietary intake of highly polyunsaturated fats represents a major source of lipid hydroperoxides in the intestinal lumen. Under conditions of high peroxide intake, excessive concentrations of lipid hydroperoxides can persist in the gut lumen and contribute to impairment of mucosal GSH-dependent detoxication pathways, enterocyte dysfunction independent of cell injury, and development of gut pathologies, including cancer. This paper summarizes our current knowledge of the determinants of intestinal lipid hydroperoxide metabolism and of the physiological and biochemical processes in lipid peroxide-mediated changes in intestinal redox status, regulation of mucosal thiol and antioxidant balance and control of intestinal cell turnover. This discussion is pertinent to understanding dietary peroxides and thiol redox balance in intestinal physiology and pathophysiology and the potential benefit of oral GSH in preserving metabolic integrity of the intestinal epithelium.
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Department of Molecular and Cellular Physiology, LSU Medical Center, Shreveport, USA.
D000818:Animals; D004220:Disulfides / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000166:cytology*; D050356:Lipid Metabolism; D009249:NADP / Q000378:metabolism; D010084:Oxidation-Reduction; D010545:Peroxides / Q000378:metabolism*; D013438:Sulfhydryl Compounds / Q000378:metabolism*
D004220:Disulfides; D010545:Peroxides; D013438:Sulfhydryl Compounds; D009249:NADP; D006861:Hydrogen Peroxide; D005978:Glutathione